KARLENE CIMPRICHSummaryAffiliation: Stanford University Country: USA Publications
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Publications
Opposing effects of the UV lesion repair protein XPA and UV bypass polymerase eta on ATR checkpoint signalingRyan D Bomgarden
Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305 5174, USA
EMBO J 25:2605-14. 2006..Taken together, these results suggest that lesion bypass and not lesion repair may raise the level of UV damage that can be tolerated before checkpoint activation, and that XPA plays a critical role in this activation...
Probing ATR activation with model DNA templatesKarlene A Cimprich
Stanford University, Department of Chemical and Systems Biology, Stanford, California 94305 5441, USA
Cell Cycle 6:2348-54. 2007..Here we discuss the implications of our findings, in the context of other recent work in the field, on our understanding of checkpoint signaling...- ATR: an essential regulator of genome integrityKarlene A Cimprich
Department of Chemical and Systems Biology, Stanford University School of Medicine, Clark Center, 318 Campus Drive, W350B, Stanford, California 94305 5441, USA
Nat Rev Mol Cell Biol 9:616-27. 2008.... - Fragile sites: breaking up over a slowdownKarlene A Cimprich
Stanford University, Department of Molecular Pharmacology, Stanford, CA 94305 5174, USA
Curr Biol 13:R231-3. 2003..Recent data suggest that these sites depend on the checkpoint kinase ATR to maintain their stability... - A requirement for replication in activation of the ATR-dependent DNA damage checkpointPatrick J Lupardus
Department of Molecular Pharmacology, Stanford University, Stanford, California 94305 5174, USA
Genes Dev 16:2327-32. 2002..These data indicate that replication is required for activation of the DNA damage checkpoint and suggest a unifying model for ATR activation by diverse lesions during S phase... - The ATR pathway: fine-tuning the forkRenee D Paulsen
Department of Chemical and Systems Biology, Stanford University, 318 Campus Drive, Stanford, CA 94305 5441, USA
DNA Repair (Amst) 6:953-66. 2007..This review summarizes our current understanding of how the ATR pathway recognizes and stabilizes stalled replication forks... - The structural determinants of checkpoint activationChristina A MacDougall
Department of Chemical and Systems Biology, Stanford University, Stanford, California 94305, USA
Genes Dev 21:898-903. 2007..These observations define the minimal DNA requirements for checkpoint activation and suggest that primed ssDNA represents a common checkpoint activating-structure formed following many types of damage... - Functional uncoupling of MCM helicase and DNA polymerase activities activates the ATR-dependent checkpointTony S Byun
Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305, USA
Genes Dev 19:1040-52. 2005.... - ATR kinase activity regulates the intranuclear translocation of ATR and RPA following ionizing radiationSharon M Barr
Department of Molecular Pharmacology, Stanford University, California 94305 5174, USA
Curr Biol 13:1047-51. 2003..These observations demonstrate that the kinase activity of ATR is essential for the irradiation-induced release of ATR and RPA from PML bodies and translocation of ATR and RPA to potential sites of DNA damage... - A genome-wide siRNA screen reveals diverse cellular processes and pathways that mediate genome stabilityRenee D Paulsen
Department of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA
Mol Cell 35:228-39. 2009..These data indicate that preservation of genome stability is mediated by a larger network of biological processes than previously appreciated... - Analyzing the ATR-mediated checkpoint using Xenopus egg extractsPatrick J Lupardus
Department of Molecular Pharmacology, Stanford University, 318 Campus Drive, Stanford, CA 94305 5441, USA
Methods 41:222-31. 2007..In addition, we describe several key assays for studying checkpoint activation as well as methods for using small DNA structures to activate ATR... - Phosphorylation of Xenopus Rad1 and Hus1 defines a readout for ATR activation that is independent of Claspin and the Rad9 carboxy terminusPatrick J Lupardus
Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305 5441, USA
Mol Biol Cell 17:1559-69. 2006..Thus, Rad1 phosphorylation provides an alternate and early readout for the study of ATR activation... - Continued primer synthesis at stalled replication forks contributes to checkpoint activationChristopher Van
Department of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA
J Cell Biol 189:233-46. 2010..These results suggest that new primers are synthesized at stalled replication forks by the leading and lagging strand polymerases and that accumulation of these primers may contribute to checkpoint activation... - Checkpoint adaptation; molecular mechanisms uncoveredPatrick J Lupardus
Stanford University, Department of Molecular Pharmacology, 318 Campus Drive, Stanford, CA 94305, USA
Cell 117:555-6. 2004..A new report in this issue of Cell by suggests the presence of a checkpoint adaptation pathway in Xenopus egg extracts that displays interesting molecular parallels to adaptation in yeast... - A novel protein activity mediates DNA binding of an ATR-ATRIP complexRyan D Bomgarden
Department of Molecular Pharmacology, Stanford University, Stanford, California 94305 5441, USA
J Biol Chem 279:13346-53. 2004.... - A cell-permeable, activity-based probe for protein and lipid kinasesMuh-ching Yee
Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305-5441, USA
J Biol Chem 280:29053-9. 2005..The biotin-wortmannin reagent is effective in the isolation of labeled proteins; all three can be used for protein labeling, and BODIPY-wortmannin is cell-permeable and can be used to label proteins within cells... - HARPing on about the DNA damage response during replicationRobert Driscoll
Department of Chemical and Systems Biology, Stanford University, Stanford, California 94305, USA
Genes Dev 23:2359-65. 2009..Knockdown of HARP results in hypersensitivity to multiple DNA-damaging agents and defects in fork stability or restart. These exciting insights reveal a key new player in the S-phase DNA damage response... - Monoubiquitination of proliferating cell nuclear antigen induced by stalled replication requires uncoupling of DNA polymerase and mini-chromosome maintenance helicase activitiesDebbie J Chang
Department of Molecular Pharmacology, Stanford University School of Medicine, 318 Campus Drive, Stanford, CA 94305 5441, USA
J Biol Chem 281:32081-8. 2006.... - Enforced proximity in the function of a famous scaffoldJames E Ferrell
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA
Mol Cell 11:289-91. 2003..Recent studies by Park, Zarrinipar, and Lim with reengineered Ste5 scaffold proteins underscore the fundamental importance of proximity in enzyme regulation and of keeping a proper distance for maintaining signaling specificity... - DNA damage tolerance: when it's OK to make mistakesDebbie J Chang
Department of Chemical and Systems Biology, Stanford University School of Medicine, Clark Center, 318 Campus Drive, W350B, Stanford, California 94305 5441, USA
Nat Chem Biol 5:82-90. 2009..Here, we discuss how two types of DNA damage tolerance, translesion synthesis and template switching, are regulated at stalled replication forks by ubiquitination of PCNA, and the conditions under which they occur... - G2 damage checkpoints: what is the turn-on?Matthew J O'Connell
Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1130, New York, NY 10029, USA
J Cell Sci 118:1-6. 2005..In this context, ATR is activated and then phosphorylates the C-terminus of Chk1, activating it to enforce a block to mitotic entry... - An ATR- and Cdc7-dependent DNA damage checkpoint that inhibits initiation of DNA replicationVincenzo Costanzo
Department of Genetics and Development, Columbia University, New York, NY 10032, USA
Mol Cell 11:203-13. 2003..The checkpoint does not require pre-RC assembly but requires loading of the single-strand binding protein, RPA, on chromatin. This is the biochemical demonstration of a DNA damage checkpoint that targets Cdc7/Dbf4 protein kinase... - Fanconi anemia proteins are required to prevent accumulation of replication-associated DNA double-strand breaksAlexandra Sobeck
Division of Biochemistry and Molecular Biology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239, USA
Mol Cell Biol 26:425-37. 2006....
Research Grants
- Regulation of the DNA damage ResponseKARLENE CIMPRICH; Fiscal Year: 2009....
- Regulation of the DNA damage ResponseKARLENE CIMPRICH; Fiscal Year: 2007....
- Role of ATR in the DNA Damage ResponseKARLENE CIMPRICH; Fiscal Year: 2006..Furthermore, they should provide important insights into human disease such as cancer and the complex process of human aging. ..
- Development of Assays for DNA Damage CheckpointsKARLENE CIMPRICH; Fiscal Year: 2003..These molecules may also be clinically useful for anti-cancer therapy, particularly when used in combination with chemotherapeutic agents that activate the DNA damage checkpoint or inhibit DNA replication. ..
- Regulation of the DNA damage ResponseKarlene A Cimprich; Fiscal Year: 2010....